TGF-β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review)

被引：138
作者：
Ye, Zhimin [1 ]
Hu, Yongbin [1 ]
机构：
[1] Cent South Univ, Basic Med Sch, Dept Pathol, 172 Tongzipo Rd, Changsha 410006, Hunan, Peoples R China
来源：
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE | 2021年 / 48卷 / 01期
基金：
中国国家自然科学基金;
关键词：
TGF-β 1; idiopathic pulmonary fibrosis; Smad; MAPK; ERK; HUMAN LUNG FIBROBLASTS; EPITHELIAL-MESENCHYMAL TRANSITION; TRANSFORMING GROWTH FACTOR-BETA(1); EXTRACELLULAR-MATRIX SYNTHESIS; ENVIRONMENTAL RISK-FACTORS; WNT/BETA-CATENIN PATHWAY; NECROSIS-FACTOR-ALPHA; P38; MAPK; MYOFIBROBLAST DIFFERENTIATION; SIGNALING PATHWAYS;
D O I：
10.3892/ijmm.2021.4965
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
Idiopathic pulmonary fibrosis (IPF) is a worldwide disease characterized by the chronic and irreversible decline of lung function. Currently, there is no drug to successfully treat the disease except for lung transplantation. Numerous studies have been devoted to the study of the fibrotic process of IPF and findings showed that transforming growth factor-beta 1 (TGF-beta 1) plays a central role in the development of IPF. TGF-beta 1 promotes the fibrotic process of IPF through various signaling pathways, including the Smad, MAPK, and ERK signaling pathways. There are intersections between these signaling pathways, which provide new targets for researchers to study new drugs. In addition, TGF-beta 1 can affect the fibrosis process of IPF by affecting oxidative stress, epigenetics and other aspects. Most of the processes involved in TGF-beta 1 promote IPF, but TGF-beta 1 can also inhibit it. This review discusses the role of TGF-beta 1 in IPF.
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页数：14
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